No abstract

The assessment and stratification of patients with chest pain in the emergency unit may indicate the appropriate therapy for each patient based on the probability of the presence of acute coronary artery disease and on the risk of its major cardiac events. That assessment is based on the triplet: clinical setting, electrocardiographic findings, and markers of myocardial lesion. We report the case of a 58-year-old male chagasic patient admitted to the emergency unit due to chest pain and palpitations, with an electrocardiogram showing sustained ventricular tachycardia and positive troponin measurement (0.99 ng/mL). The patient underwent cine coronary angiography, which evidenced no obstructive coronary artery disease.

We read with great interest the article by L. Kritharides and J. Vohra on "Late development of conduction block over the Mahaim fibers after electrical atrioventricular junction ablation for Mahaim fiber tachycardia" (PACE, 1992; 15:256-261). However, their Figure 2 may be interpretable in a different way. In their interpretation, an RV extrastimulus advanced QRS by only 10 msec but prolonged VA conduction by 35 msec (60 msec -» 95 msec). If this were true, atrial cycle length encompassing the RV extrastimulus should have been lengthened from 300 msec to 325 msec by 25 msec (35 msec -10 msec = 25 msec). But the atrial cycle length on HRA and PCS encompassing the RV extrastimulus is 300 msec (according to our measurement), indicating that the RV extrastimulus most probably did not penetrate the tachycardia circuit. If one were to assume that the RV extrastimulus delayed the activation of the low septal right atrium on HBE alone by 25 msec, shortening by 25 msec in intraatrial conduction time between the low septal right atrium to HRA and PCS would have to occur, which would be unlikely. It seems to us that exact measurement of VA conduction time on HBE in Figure 2 is very difficult in consideration of the very sinall atrial deflection on HBE during sinus beat (last beat in Fig. 2).We thank Drs. Suzuki and Hiejima for their comments on Figure 2 in our article. They are quite correct in their observation that the atrial cycle length encompassing the right ventricular extrastimulus (RVES) is not lengthened by 25 msec and their suggestion that the RVES did not penetrate the tachycardia circuit is certainly a valid one.The diagnosis of Mahaim fiber tachycardia in this patient is beyond doubt. Our inference that RVES penetrated the tachycardia circuit is based on prolongation of the tachycardia cycle length (by 20 msec in the surface ECC and 35 msec in RV electrogram) and consistent termination of tachycardia by only slightly premature right ventricular extrastimuli. It would have, of course, been ideal to measure the VH interval in the HBE tracing for confirmation of retrograde delay by RVES; however, that was not possible here.